关键词: 短链脂肪酸, 肥胖, 糖脂代谢, 脂肪肝

Abstract: Objective To observe the effects of short chain fatty acids (SCFAs) on metabolism of glucose and lipid in obese mice induced by high fat diet (HFD), and to investigate the possible mechanisms from the perspective of intestinal epithelial barrier function. Methods Forty C57BL/6J mice were equally randomly divided into normal diet (ND) group, HFD model group, SCFAs treatment (HFD+SCFAs) group and lactulose (LA) treatment (HFD+LA) group. Mice were fed a HFD for 14 weeks, and treated with corresponding drugs or distilled water since week 10. After 4-week treatment, mice were sacrificed for observing body weight, food intake, liver weight, ratio of liver weight to body weight, morphology and diameter of adipocytes after epididymis, fasting plasma glucose (FBG), fasting serum insulin (FINS), homeostatic model assessment insulin resistance (HOMA-IR), serum triglyceride (TG), serum cholesterol (TC), low density lipoprotein, hepatic TG, serum alanine aminotransferase, aspartate aminotransferase, and hepatic and colonic tissue pathological changes. Results The body weight, liver weight, ratio of liver weight to body weight, FBG, FSI, HOMA-IR, serum TG, serum TC and hepatic TG in HFD+SCFAs group were significantly lower than those in the HFD group (P<0.01). SCFAs was superior to LA in reducing FSI, HOMA-IR, serum TG, serum TC, and hepatic TG (P<0.01 or P<0.05). Moreover, hepatic steatosis, inflammation and ballooning were significantly improved in HFD+SCFAs group than those in HFD group, and disease activity score was decreased (P<0.01). SCFAs intervention could significantly improve colonic pathology, including colonic epithelial damage, glandular disorder and inflammatory cell infiltration induced by HFD. Conclusion SCFAs can effectively reduce body weight, improve the metabolism of glucose and lipid and decrease hepatic fat deposition in obese mice induced by HFD. Reducing intestinal inflammatory response and enhancing intestinal epithelial barrier function maybe one of the possible mechanisms.

Key words: Short chain fatty acids, Obesity, Metabolism of glucose and lipid, Fatty liver